TLR2 and diabetes mellitus: The interaction of phagocytes with apoptotic or secondary necrotic β-cells has been suggested to induce the initial response by stimulating the priming of diabetogenic T- cells in a TLR2-dependent manner, as genetic deletion of TLR2, but not TLR4, significantly reduced diabetes incidence in NOD mice, as well as in mice treated with STZ [10].